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Although NK cells are usually considered to be morphologically large granular lymphocytes, the malignant NK cells in this case were agranular and blast-like, resembling human blastic NK cell leukaemia.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Indolent NK-cell lymphoproliferative disorder, also known as chronic natural killer (NK) cell large granular lymphocytosis (leukemia), is a very rare entity in the World Health Organization (WHO) Classification of Tumors of Hematopoietic & Lymphoid Tissues.

Unlike aggressive NK-cellleukemia, which is malignant, the WHO does not specify whether indolent NK-cell lymphoproliferative disorder is reactive or neoplastic.

Patients with indolent NK-cell lymphoproliferative disorder are usually asymptomatic older adults who have a nonprogressive, very stable clinical course.

We report an unusual case of an aggressive extranodal NK-celllymphoma, non-nasal type, which presented as a subcutaneous tissue mass, which apparently transformed from a preexisting, untreated indolent NK-cell lymphoproliferative disorder in an 65-year-old otherwise healthy white man.

The extranodal NK-celllymphoma and the NK-cell lymphoproliferative disorder in the blood and bone marrow share a distinctive and identical NK-cell immunophenotype and genotype: CD56/CD8/TIA-1-positive and surface CD3-negative, negative for Epstein-Barr virus infection, and no evidence of T-cell and B-cell receptor gene rearrangements.

To the best of our knowledge, such aggressive lymphomatous transformation in an indolent NK-cell lymphoproliferative disorder has not been previously reported.

This study also indicates that HLA-G5 soluble isoform remains evenly distributed in the cytoplasm of M8-HLA-G5 conjugated to NKL cells, suggesting that HLA-G5 does not require to polarize toward effector cell to induce efficient inhibition.

These results highlight the inhibitory mechanisms mediated through HLA-G5 leading to tumor escape from NK cell cytotoxicity.

The authors reviewed the literature on natural killercell neoplasm and compared the clinical characteristics, natural history, and association of Epstein-Barr virus infection with hemophagocytic syndrome.

In this study, we first examined the effects of 2-arachidonoylglycerol on the motility of human natural killer cells.

The migration of natural killer cells induced by 2-arachidonoylglycerol was abolished by treating the cells with SR144528, a CB2 receptor antagonist, suggesting that the CB2 receptor is involved in the 2-arachidonoylglycerol-induced migration.

It is conceivable that the endogenous ligand for the cannabinoid receptor, that is, 2-arachidonoylglycerol, affects natural killercell functions such as migration, thereby contributing to the host-defense mechanism against infectious viruses and tumor cells.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title]NK-cell neoplasms in Japan.

Neoplasms putatively originating from precursor and mature natural killer (NK) cells are rare, and their clinical features are unclear.

A nationwide survey was performed in Japan to clarify the clinical features of these neoplasms diagnosed between 1994 and 1998, and data for 237 patients who met the criteria for putative NK cell-lineage neoplasms were analyzed.

The median overall survival time of patients with aggressive NK-cellleukemia/lymphoma was 2 months, which for chronic NK lymphocytosis was more than 8 years, and that for the other types of NK-cell neoplasms was between 6 and 22 months.

Nasal NK-celllymphoma and extranasal NK-celllymphoma share the same histology.

The age of affliction was the same, but the sex was different with males predominantly having nasal NK-celllymphoma and females extranasal NK-celllymphoma.

Patients with extranasal NK-celllymphoma had the tendency to exhibit a more advanced state of disease, with significantly higher International Prognostic Index and LDH levels, and significantly lower hemoglobin and platelet levels.

Precursor NK-cell acute lymphoblastic leukemia and blastic NK-celllymphoma were arbitrarily defined by the presence or absence of 30% or more of blastic cells in the bone marrow or peripheral blood, but there were no significant differences for affected age, gender, involved sites or prognosis.

Aggressive NK-cellleukemia/lymphoma and extranasal NK-celllymphoma were arbitrarily defined by the presence or absence of 30% or more of large granular lymphocytes in the bone marrow or peripheral blood and it is possible that aggressive NK-cellleukemia/lymphoma is a leukemic phase of extranasal NK-celllymphoma.

The incidence of skin involvement, however, was significantly higher for extranasal NK-celllymphoma, suggesting that the two diseases are different.

In nasal NK-celllymphoma, Epstein-Barr virus in tumor cells was detected in all patients tested, suggesting its causative role.

Despite recent advances in NK-cell research, which have expanded our understanding of the biology of NK-cell neoplasm, it cannot yet be sharply delineated from myeloid neoplasms and T-cell neoplasms even in some "well-known" entity, such as extranodal NK/T-celllymphoma.

This review describes current knowledge of the biology of NK cells and pathology of NK neoplasms as classified in the 2008 WHO classification of tumours of hematopoietic and lymphoid tissues.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title]Aggressivenatural killercellleukemia: is Epstein-Barr virus negativity an indicator of a favorable prognosis?

Aggressivenatural killer (NK) cellleukemia (ANKL) is a prototype of an Epstein-Barr virus (EBV)-associated lymphoid malignancy, which is characterized by a fulminant clinical course and a median survival interval <2 months.

In conclusion, EBV-negative ANKL is an uncommon malignancy that pursues a less aggressive clinical course than EBV-positive ANKL.

Because geldanamycin (GA) and its derivative, 17-allylamino-17-demethoxygeldanamycin (17-AAG), exhibit anti-tumour activity by degrading HSP90 client proteins, including Akt, we investigated the effect of GA and 17-AAG on the survival of NKTL cell lines.

EBV-positive NKTL cell lines, Hank-1 and NK-YS, and an EBV-negative NK leukaemia cell line, NK-L, were treated with PI3K and Akt inhibitors, GA, and 17-AAG, and were subjected to apoptosis and cell viability assays, and immunoblot analysis.

22. Slater DN: The new World Health Organization-European Organization for Research and Treatment of Cancer classification for cutaneous lymphomas: a practical marriage of two giants.Br J Dermatol; 2005 Nov;153(5):874-80[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The new classification will facilitate more uniformity in diagnosis, management and treatment of cutaneous lymphomas.

In particular, it provides a useful distinction between indolent and more aggressive types of primary cutaneous lymphoma and provides practical advice on preferred management and treatment regimens.

Natural killer (NK) cell lymphomas/leukemias are highly aggressive lymphoid malignancies, but little is known about their genomic alterations, and thus there is an urgent need for identification and analysis of NK cell lymphomas/leukemias.

We performed an array CGH analysis for 27 NK-celllymphoma/leukemia cases that were classified into two disease groups based on the World Health Organization Classification (10 aggressive NK-cellleukemia cases and 17 extranodal NK/T-cell [NK/T] lymphomas, nasal type).

The recurrent regions characteristic of the aggressive NK-cellleukemia group compared with those of the extranodal NK/T lymphoma, nasal-type group, were gain of 1q and loss of 7p15.1-p22.3 and 17p13.1.

Recurrent regions characteristic of the extranodal NK/T lymphoma, nasal-type group, compared with those of the other group were gain of 2q, and loss of 6q16.1-q27, 11q22.3-q23.3, 5p14.1-p14.3, 5q34-q35.3, 1p36.23-p36.33, 2p16.1-p16.3, 4q12, and 4q31.3-q32.1.

Our results can be expected to provide further insights into the genetic basis of lymphomagenesis and the clinicopathologic features of NK-cell lymphomas/leukemias.

Although NK-YS and NK-92 were highly resistant to various anti-tumour agents, l-asparaginase induced apoptosis in these two NK-cell lines.

Samples of chronic NK lymphocytosis, an NK-cell disorder with an indolent clinical course, were resistant to both drugs.

Our study clearly separated two major categories of NK-cell disorders and ALL according to the sensitivity to DXR and l-asparaginase.

At least in nasal-type NK-celllymphoma, there was a good correlation among asparagine synthetase expression, in vitro sensitivity and clinical response to l-asparaginase.

In aggressive NK-cell leukaemia, although asparagine synthetase expression was high at both mRNA and protein levels, l-asparaginase induced considerable apoptosis.

We confirmed rather specific anti-tumour activity of l-asparaginase against NK-cell tumours in vitro, which provides an experimental background to the clinical use of l-asparaginase for NK-cell tumours.

The uniform and aberrant phenotype of NK cells with infiltration of bone marrow and spleen was in keeping with a malignant diagnosis.

We discuss the difficulties in the diagnosis of this condition, explore possible causes of cytopenia(s), and highlight the role of immunosuppression in controlling disease manifestations in large granular lymphocyte proliferative disorders.

We found methylation of the first exon of the p16INK4A gene in two cases (one aggressive, one blastic), and methylation of the p14ARF gene in one aggressive NK cellleukemia.

MS-PCR suggested that the p73 and p21 genes were methylated in seven cases, respectively (p73: one blastic, one nasal, five chronic; p21: one myeloid/NK, one aggressive, one nasal, and four chronic); bisulfite sequencing confirmed that methylated alleles of these genes were dominant in the samples except three cases (one myeloid/NK, one aggressive, and one chronic) in which methylated alleles of the p21 genes were less than 34% of all alleles.

These results suggested that inactivation of the cell cycle regulatory genes by DNA methylation could be associated with tumorigenesis in NK cell disorders, not only aggressive subtypes but also chronic subtype.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Immunophenotypic features in leukemia of NK cell series].

The aim was to investigate the immunophenotypes of NK series leukemia.

Immunophenotypes of 297 cases of acute leukemia (AL) were measured by flow cytometry, and these immucopenotypic features were analyzed.

6 cases were NK series leukemia and 37 cases were acute myelogenous leukemia with CD56 expressed.

One patient has been diagnosed as myeloid/NK cell precursor acute leukemia, two patients were blastic NK cellleukemia, one was supposed to be NK-like T-celllymphoma/leukemia, while another one was large granular lymphocyte leukemia (LGLL).

It is concluded that almost all of CD56 positive leukemia were acute myelogenous leukemia with CD56 expressed.

The immunophenotypes of NK series leukemia were antigens from hematopoietic stem cells to T/NK progenitor cells with meyloid antigen positive, and through NK progenitors to mature NK cells.

The immunophenotypes of heterogeneous NKleukemia cells are different, that should be carefully distinguished.

They manifest a distinct biologic behavior that ranges from indolent to very aggressive.

RESULTS: Sustained LGLs, characteristic immunophenotype, clonal origin of leukemic cells, and clinical presentation are the most important features that distinguish indolent from aggressive subtypes of LGL leukemia and guide the selection of therapy.

Patients with symptomatic indolent T-cell or NK-cellLGL leukemia are usually treated with immunosuppressive therapies in contrast to aggressive T-cell and NK-cellLGL leukemia, which require intensive chemotherapy induction regimens.

CONCLUSIONS: Future scientific advances focusing on the delineation of molecular pathogenic mechanisms and the development of new targeted therapies for each distinct LGL leukemia entity should lead to improved outcomes of patients with these disorders.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Precursor natural killercellleukemia.

Natural killer (NK) cell tumors are a rare and heterogeneous group of disorders.

Immature NK cell tumors are less common, and are less recognized and defined than mature NK cell tumors.

There is insufficient experience of diagnosis and treatment with immature NK cell tumors, especially in pediatric patients.

Here we describe a pediatric patient with precursor NK cellleukemia and review the literature of the previously reported cases in children to further help characterize the diagnosis, treatment, and outcome.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Retrospective analysis of 4 cases of the so-called blastic NK-celllymphoma, with reference to the 2008 WHO classification of tumours of haematopoietic and lymphoid tissues].

OBJECTIVE: To study the clinical and pathologic features of 4 cases of the so-called blastic natural killer (NK)-celllymphoma, with reference to the 2008 WHO classification of tumours of haematopoietic and lymphoid tissues.

METHODS: The clinical, pathologic and immunohistochemical findings (EliVision method) of 4 cases of blastic NK-celllymphoma (previously diagnosed according to the 2001 WHO classification) were retrospectively analyzed and reclassified with a special reference to the 2008 WHO classification.

RESULTS: The 4 cases of hematologic malignancy studied were characterized by the presence of medium-sized blastic lymphoma cells, CD56 expression, and absence of lineage-specific B-cell, T-cell and myeloid cell markers.

According to the 2001 WHO classification, they fell into the category of blastic NK-celllymphoma.

They are likely derived from the plasmacytoid dendritic cells rather than NK cells.

They were then, according to the 2008 WHO classification, reclassified as the blastic plasmacytoid dendritic cell neoplasm.

This case was provisionally classified as a ambiguous lineage leukemia-NK cell lymphoblastic leukemia/lymphoma.

CONCLUSIONS: The so-called blastic NK-cell lymphomas in the 2001 WHO classification are rare and represent a heterogeneous group of lymphoproliferative disorders, with different clinical, pathologic and immunohistochemical features.

We describe a 44-yr-old Japanese woman with persistent polyclonal T-cell proliferation and recalcitrant clinical course of haemophagocytic syndrome (HPS).

Aggressivenatural killercell leukaemia (ANKL) without an association with Epstein-Barr virus was detected 1 month after therapeutic splenectomy that followed 3 yr of immunosuppressive therapy against HPS.

The immunophenotype of these leukaemia cells was CD56, CD16(dim), CD7, CD45RA and they expressed some CD2, CD8 and HLA-DR.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Natural killer (NK) cell neoplasms, which include extra-nodal NK/T-celllymphoma (nasal and extra-nasal) and aggressive NK cell leukaemia, are generally rare, but they are more common in people of Oriental, Mexican and South American descent.

These neoplasms are highly aggressive, and show a strong association with Epstein-Barr virus.

Aggressive NK cell leukaemia affects younger patients, who present with poor general condition, fever, and disseminated disease; they often die within a short time from systemic disease or complications such as multi-organ failure.

Aggressive NK cell leukaemia must be distinguished from T-cell large granular lymphocyte leukaemia and indolent NK cell lympho-proliferative disorder, both of which are indolent.

We present a case of young Asian male with aggressive NK cell leukaemia who presented with a poor general condition and disseminated disease.

The patient had a rapidly progressive disease and died within weeks of diagnosis.

The diagnosis is proven by the monoclonal proliferation of EBV-infected T or NK cells, which is a time-consuming and complicated method.

T-cell monoclonality is helpful for the screening of EBV-infected T-cell LPD in patients with EBV-genome burden and is easily shown with T-cell-receptor rearrangement or the T-cell repertoire, whereas NK-cell monoclonality is difficult to prove due to its lacking such rearranged receptors.

We investigated a set of killer immunoglobulin-like receptors (KIRs) and also CD94-NKG2 heterodimers on NK cells, namely the NK-cell repertoire.

Skewed repertoires were seen in all patients with EBV-infected NK-cell LPD, but not in any patients with EBV-infected T-cell LPD and were restored only after successful treatment.

The normal KIR repertoire is variable for each individual and it seems difficult to detect minimal residual EBV-infected lymphocytes.

However, the NK-cell repertoire is feasible for identifying EBV-infected NK-cell LPD and evaluating the treatment effect.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Here, we show that MUC16, a heavily glycosylated 3-5 million Da mucin expressed on the surface of ovarian tumor cells, inhibits the formation of immune synapses between NK cells and ovarian tumor targets.

RESULTS: Expression of low levels of MUC16 strongly correlated with an increased number of conjugates and activating immune synapses between ovarian tumor cells and primary naïve NK cells.

In primary leukemia cells analyzed ex vivo, we found GC-resistant leukemia cells in three out of seven patients with acute myeloid leukemia and one out of six patients with acute lymphoblastic leukemia.